Thr181
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Home > Phosphorylation Site Page: > Thr181  -  RARA (human)

Site Information
CSESYTLtPEVGELI   SwissProt Entrez-Gene
Blast this site against: NCBI  SwissProt  PDB 
Site Group ID: 455328

In vivo Characterization
Methods used to characterize site in vivo:
immunoprecipitation ( 1 ) , mutation of modification site ( 1 , 2 ) , phospho-antibody ( 1 ) , western blotting ( 1 , 2 )
Disease tissue studied:
liver cancer ( 1 ) , hepatocellular carcinoma ( 1 ) , lung cancer ( 2 ) , non-small cell lung cancer ( 2 )
Relevant cell line - cell type - tissue:

Upstream Regulation
Putative in vivo kinases:
JNK1 (human) ( 1 )
Kinases, in vitro:
JNK1 (human) ( 2 )
Treatments:
anisomycin ( 1 ) , SP600125 ( 1 )

Downstream Regulation
Effects of modification on RARA:
protein degradation ( 1 , 2 ) , ubiquitination ( 1 , 2 )
Effects of modification on biological processes:
signaling pathway regulation ( 1 )

References 

1

Hoshikawa Y, et al. (2011) c-Jun N-terminal kinase activation by oxidative stress suppresses retinoid signaling through proteasomal degradation of retinoic acid receptor α protein in hepatic cells. Cancer Sci 102, 934-41
21272161   Curated Info

2

Srinivas H, et al. (2005) c-Jun N-terminal kinase contributes to aberrant retinoid signaling in lung cancer cells by phosphorylating and inducing proteasomal degradation of retinoic acid receptor alpha. Mol Cell Biol 25, 1054-69
15657432   Curated Info